IN-DEPTH: RACING-RELATED LAMENESS


eliminates the natural stimulation of circulation that would best support repair. We see the result of this perturbation of the horse’s natural routine as the accumulation of edema within the distal limb (“stocking up”) of the horse when they are stall- confined for long periods of time after intense exer- cise. We circumvent the edema with the application of “stall bandages” to reduce the edema or “stocking up.” The elimination of the edema eliminates the clinical symptom but does not resolve the primary condition of accumulated damage to the bones of the distal limb of the horse. Returning the horse to the natural grazing environment for at least 8 hours of every 24 for a 2- to 3-month period of time resolved the clinical lameness seen with the repeti- tive cyclic loading and allowed a return to racing in 95% of the horses treated.27 Another man-made predisposition to subchondral


bone injury in the distal metacarpus is the addition of the excessive “toe grab” in the Thoroughbred race- horse.28 The toe grab adds a braking affect to the impact of the horse’s foot in the traditional dirt- racing surface. Experiments with instrumented shoes have shown that the forces that these horses receive at the impact of the foot with a toe grab into the traditional racing surface exceed the load re- ceived with weight-bearing.29 The toe grab in- creases the resistance to slide of the foot in the forward direction and causes the toe to turn down into the loose cushion of the classic dirt-racing sur- face. Lowering the toe creates a functional eleva- tion of the heel of the foot, which then translates into a reciprocal increase in extension within the fetlock. Hyperextension of the fetlock joint increases the load on the suspensory apparatus and the palmar/ plantar articular surface of the cannon bone at its interface with the sesamoid bone. This increased load increases the damage to the subchondral bone, cyclically producing damage in excess of repair, bruising, and structural damage to the articular surface of the fetlock joint in this location.20,30 Because the articular surface has a limited means to adapt (because it cannot change its shape), this leads to the myriad of clinical lameness encountered as a result of this process if training continues, pro- ceeding faster than the horse can adapt. The same forces will be in play on other surfaces such as turf or artificial racing surfaces, but experimental stud- ies have shown that the magnitude is greatest on the traditional dirt racing surface.30 This syn- drome at least partly explains the high incidence of injury to the third metacarpus of the racehorse fet- lock joint when compared with other articulations of the distal limb. Recent questions have surfaced as to whether we


could have inadvertently altered the genetic mate- rial and the bone’s ability to adapt by selective breeding, increasing the predisposition of the horse to injury. Progressive decrease in the number of races per year completed by the North American Thoroughbred seems to raise the question, but


closer examination indicates the economics of racing are probably a bigger driver of the decreases in starts than the question of soundness.b Publication of trainers’ statistics concerning the percentage of horses that finish in the top three places and the continual growth of the expense concerned with training without a similar growth in purses encour- ages more selective entry of horses in races. This increases the amount of training, and the participa- tion in a race occurs only when the connections feel the horse is at peak form. Emphasis on the horse’s value as breeding stock also promotes the level of performance rather than the number of races com- peted. These economic pressures continually re- duce the emphasis on career longevity and reward early retirement with lucrative breeding careers. One would suspect that the emphasis on early ca- reer “brilliance” and the de-emphasis of longevity would eventually take a toll on the ability to the racehorse to produce durable skeletons and long- lived careers. In summary, bone is not a purely structural inert material; it is a dynamic support tissue that adapts to the work it is asked to do. Most clinical diseases are the result of training and damage in excess of the horse’s ability to respond to the exercise stimu- lus. Understanding of the horse’s bone response to exercise and modulation and adaptation of exercise programs to individual horses and to their response to the stimulus greatly aids in the avoidance of injury in the equine athlete.


References and Footnotes


1. Cornelissen BP, van Weeren PR, Ederveen AG, et al. Influ- ence of exercise on bone mineral density of immature cortical and trabecular bone of the equine metacarpus and proximal sesamoid bone. Equine Vet J Suppl 1999:79–85.


2. Cullinane DM. The role of osteocytes in bone regulation: mineral homeostasis versus mechanoreception. J Musculo- skelet Neuronal Interact 2002;2:242–244.


3. Teti A, Zallone A. Do osteocytes contribute to bone mineral homeostasis? Osteocytic osteolysis revisited. Bone 2009;44: 11–16.


4. Nunamaker DM, Butterweck DM, Provost MT. Some geo- metric properties of the third metacarpal bone: a compari- son between the Thoroughbred and Standardbred racehorse. J Biomech 1989;22:129–134.


5. Sherman KM, Miller GJ, Wronski TJ, et al. The effect of training on equine metacarpal bone breaking strength. Equine Vet J 1995;27:135–139.


6. Nicholson CL, Firth EC. Assessment of bone response to conditioning exercise in the radius and tibia of young Thor- oughbred horses using pQCT. J Musculoskelet Neuronal In- teract 2010;10:199–206.


7. Firth EC, Rogers CW, van Weeren PR, et al. Changes in diaphyseal and epiphyseal bone parameters in Thoroughbred horses after withdrawal from training. J Musculoskelet Neuronal Interact 2007;7:74–76.


8. Firth EC, Delahunt J, Wichtel JW, et al. Galloping exercise induces regional changes in bone density within the third and radial carpal bones of Thoroughbred horses. Equine Vet J 1999;31:111–115.


9. Lanyon LE. Osteocytes, strain detection, bone modeling and remodeling. Calcif Tissue Int 1993;53(Suppl 1):S102–106.


10. Nunamaker DM, Butterweck DM, Provost MT. Fatigue fractures in Thoroughbred racehorses: relationships with


AAEP PROCEEDINGS  Vol. 59  2013 421


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